Radon treatment is used as an established therapy option in chronic painful inflammatory diseases. While analgesic effects are well described, little is known about the underlying molecular effects. Among the suspected mechanisms are modulations of the anti-oxidative and the immune system. Therefore, we aimed for the first time to examine the beneficial effects of radon exposure on clinical outcome as well as the underlying mechanisms by utilizing a holistic approach in a controlled environment of a radon chamber with an animal model: K/BxN serum-induced arthritic mice as well as isolated cells were exposed to sham or radon irradiation. The effects on the anti-oxidative and the immune system were analyzed by flow-cytometry, qPCR or ELISA. We found a significantly improved clinical disease progression score in the mice, alongside significant increase of peripheral blood B cells and IL-5. No significant alterations were visible in the anti-oxidative system or regarding cell death. We conclude that neither cell death nor anti-oxidative systems are responsible for the beneficial effects of radon exposure in our preclinical model. Rather, radon slightly affects the immune system. However, more research is still needed in order to fully understand radon-mediated effects and to carry out reasonable risk-benefit considerations.
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http://dx.doi.org/10.3390/cells11040689 | DOI Listing |
Asia Pac J Clin Oncol
January 2025
Wellington Blood and Cancer Centre, Health New Zealand/Te Whatu Ora - Capital, Coast and Hutt Valley, Wellington, New Zealand.
Aim: Manatū Hauora, the Ministry of Health of New Zealand (NZ), published minimum standards for molecular testing of colorectal cancers (CRCs) in June 2018. These included mismatch repair (MMR) testing at diagnosis and BRAFV600E mutation analysis on newly diagnosed stage IV CRCs. This study aimed to determine the proportion of patients with CRC in the South Island of NZ with metastatic deficient mismatch repair (dMMR) CRC, the proportion of metastatic CRCs and dMMR CRCs that have a BRAFV600E mutation, and audit testing for BRAF mutations and appropriate referral to genetics services.
View Article and Find Full Text PDFMiddle East J Dig Dis
October 2024
Department of Pediatrics, All India Institute of Medical Sciences (AIIMS), Bhopal, Madhya Pradesh, India.
Celiac disease (CD) is an immune-mediated enteropathy with varied systemic involvement and association with increased morbidity and mortality. Strong clinical suspicion is the key, and diagnosis is made using histopathology and serology. Though the consumption of a strict gluten-free diet can improve symptoms and limit mucosal damage, curative therapy is still lacking.
View Article and Find Full Text PDFCureus
January 2025
Emergency Medicine, University Hospitals St. John Medical Center, Westlake, USA.
Autoimmune hemolytic anemia (AIHA) is a condition that causes an individual's immune system to destroy its own red blood cells. Immune cells are activated against the red blood cell antigens to induce hemolysis. Patients typically present with symptomatic anemia when the extent of hemolysis overcomes the bone marrow's ability to compensate.
View Article and Find Full Text PDFActa Pharm Sin B
December 2024
School of Pharmacy, Institute of Hepatology and Metabolic Diseases, Department of Hepatology, the Affiliated Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou 311121, China.
Specific tumor-targeted gene delivery remains an unsolved therapeutic issue due to aberrant vascularization in tumor microenvironment (TME). Some bacteria exhibit spontaneous chemotaxis toward the anaerobic and immune-suppressive TME, which makes them ideal natural vehicles for cancer gene therapy. Here, we conjugated ZIF-8 metal-organic frameworks encapsulating eukaryotic murine interleukin 2 () expression plasmid onto the surface of VNP20009, an attenuated strain with well-documented anti-cancer activity, and constructed a TME-targeted delivery system named /ZIF-8@.
View Article and Find Full Text PDFActa Pharm Sin B
December 2024
Department of Molecular and Life Science, Hanyang University, Ansan 15588, Republic of Korea.
The pathophysiology of sepsis is characterized by a systemic inflammatory response to infection; however, the cytokine blockade that targets a specific early inflammatory mediator, such as tumor necrosis factor, has shown disappointing results in clinical trials. During sepsis, excessive endotoxins are internalized into the cytoplasm of immune cells, resulting in dysregulated pyroptotic cell death, which induces the leakage of late mediator alarmins such as HMGB1 and PTX3. As late mediators of lethal sepsis, overwhelming amounts of alarmins bind to high-affinity TLR4/MD2 and low-affinity RAGE receptors, thereby amplifying inflammation during early-stage sepsis.
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